Maynard, MA, USA: Beacon-Villager newspaper column on local history, observations on nature and recreational activities, plus an occasional health-related article. Columns from 2009-11 collected into book "MAYNARD: History and Life Outdoors." Columns from 2012-14 collected into book "Hidden History of Maynard." - David A. Mark

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Tuesday, August 6, 2013

Deer Ticks and Lyme Disease

This is a reposting of a 2011 article, revised, because we are once again in Lyme disease season. See also the anaplasmosis article posted in August 2013 (another tick borne bacteria).NEWS FLASH: On August 18, 2013, the Centers for Disease Control revised its estimates of numbers of new cases per year from 30,000 to 300,000. This 10X increase was the result of survey blood testing laboratories for numbers of positive blood tests, versus the old method of depending on reports from physicians. All physicians are supposed to report all confirmed or suspected Lyme disease to the CDC, but obviously, this has not been true.

Why “Lyme?” Names can be for symptoms, the discovering
doctor’s name, a defining population or a place. The villages of Old Lyme and
Lyme, in Connecticut,
combined population under 10,000, were the epicenter of an unknown disease in
1975. The story starts with a mother. Polly Murray had two children diagnosed
with juvenile rheumatoid arthritis. As she commiserated with other parents of
children with JRA, she was struck by how common this supposedly rare condition
had become in their small community. Murray
complained to the state health department, thinking perhaps there was an
unknown pollution problem.

Her efforts and her list of 39 children with
similar symptoms brought in Dr. Snydman of the health department, who brought
in rheumatology expert Dr. Allen Steere from YaleUniversity.
Dr. Steere made the connection to the possibility of tick-borne bacterial
disease. The bacteria responsible for Lyme disease is Borrelia burgdorferi. Lyme Arthritis,
later renamed Lyme disease, could have as easily been Murray’s disease or
Steere’s disease.

A tick’s life has three stages played out over two years. Confusingly,
people describe deer ticks as the size of a typed dot, a poppy seed, or an
apple seed. All descriptions are true. Uninfected larvae hatch from eggs
in late spring, hoping to latch on to a field mouse. One blood meal is all they
are after, but if the mouse host is infected, so becomes the tick. The larval
tick morphs into the nymph stage and forgoes feeding off animals through fall,
winter, and early spring. Come May, these poppy seed sized, possibly infected
nymphs are hanging out on ground level vegetation, hoping for a mouse or bird
to brush by.

Ground level gardening work puts humans at risk. Most human
infections are from nymphs, contracted May through August. The nymph stage is
also after only one modest-sized blood meal, so it does not stay attached for long. Gorged, the ticks drop off the host to the
ground and morph into adults. Come fall, these adults climb tall grasses and
shrubbery to pose there legs outstretched, hoping to latch onto a passing deer.
Once on board, females adult settle in for their third and last blood meal, getting the protein they need to make eggs,
while males wander around to find and mate with the females. It helps to
visualize each deer as a singles cruise ship.

Females overwinter at ground
level, then in the spring lay 1,000 to 3,000 eggs to start the cycle over again.
Some adults miss latching onto a deer in the fall, overwinter as adults, and
are then out in spring for a last chance at mating and a blood meal (and an infection). More
information is available from the American Lyme Disease Foundation [www.aldf.com] or the Centers for Disease Control [http://www.cdc.gov/ticks/]. ALDF has a good pictoral of the life cycle and high risk months at www.aldf.com/DeerTickEcology.shtml.

Trans-species diseases are evolution’s biggest wild card. In
theory, diseases are not supposed to eliminate their hosts. Or rather, those
that do disappear from the global gene pool along with their hosts – game over.
The norm is more like disease, resistance, mutating disease, mutating
resistance, ad infinitum. Both
survive. More rarely, a disease jumps species.
American chestnut trees, elms and dogwoods all succumbed to non-native
diseases. Sheep scabies passed through cows to give us the gift of mad cow
disease. The influenza virus drifts across humans, pigs and ducks, wreaking
havoc as it mutates. Natural hosts for Lyme disease bacteria are field mice and
whitetail deer. Humans are just collateral damage.

No deer means no deer ticks, means no Lyme disease. Extensive
land clearing, farming and hunting forced the U.S. whitetail deer population to
under half a million a century ago. Subsequent establishment of controlled
hunting seasons, loss of natural predators, plus abandonment of many eastern
farms to reforestation has resulted in an out-of-control population exceeding
twenty million deer.

While wildlife biologists consider 10 deer per square mile
a sustainable population, many northeastern states are seeing 40 to 60 or
higher per square mile in rural and suburban areas. Lyme disease cases in the U.S. increased
from 10,000 in 1992 to 30,000 in 2012. Of that last total, more than two-thirds
were in the New England and mid-Atlantic
states. One could argue that not going into the woods is an
answer, but as any gardener, landscaper or farmer knows, the deer have
come to us.